Neonatal Chest Imaging

Eric J. Crotty

Contents

1 Introduction .......................................................................... 173

2 Technique.............................................................................. 173

3 Systematic Approach........................................................... 174

4 Medical Disease.................................................................... 1764.1 Transient Tachypnea of the Newborn .................................. 1764.2 Respiratory Distress Syndrome............................................. 1764.3 Bronchopulmonary Dysplasia ............................................... 1804.4 Meconium Aspiration Syndrome .......................................... 1824.5 Neonatal Pneumonia.............................................................. 183

5 Air Leak Phenomenon ........................................................ 1875.1 Pulmonary Interstitial Emphysema....................................... 1875.2 Pneumothorax ........................................................................ 1885.3 Pneumomediastinum.............................................................. 1895.4 Pneumopericardium ............................................................... 189

6 Lines and Tubes................................................................... 189

7 Summary............................................................................... 194

References ...................................................................................... 194

Abstract

Neonatal lung disease is a common problem with potentialfor significant morbidity and mortality. Chest radiographsremain the most important imaging tool for investigationof these diseases. Many of these diseases can have asimilar appearance on radiographs, but differentiation canbe often be achieved by noting differentiating andsometimes subtle imaging findings, and taking intoconsideration pertinent clinical information such as thegestational age and perinatal history. As these patients areoften critically ill, radiographs also need to be evaluatedfor adequate positioning of the support tubes and cathe-ters. Many complications of these diseases, such as air leakrelated to mechanical ventilation, can also be assessedwith radiographs. This chapter will describe and illustratethe imaging findings of diseases of the neonatal lung andcomplications of their management.

1 Introduction

The chest radiograph is the most frequent imaging studyperformed on neonates. This reflects respiratory distressbeing a very common sign in an ill neonate, especially inpremature infants. A wide spectrum of medical and surgicaldisorders can present in the neonatal period with respiratorydistress. This chapter will focus on the common pulmonaryconditions, as the cardiac and surgical conditions will bediscussed in other chapters.

2 Technique

Although the radiation dose from an individual chest radio-graph is low, it is important that the ALARA principals areobserved. While patients in the neonatal intensive care unitare ill, they often do not require a daily chest radiograph, and

E. J. Crotty (&)Department of Radiology,Cincinnati Children’s Hospital Medical Center,University of Cincinnati College of Medicine,3333 Burnet Avenue, Cincinnati, OH 45229-3039, USAe-mail: eric.crotty@cchmc.org

P. Garcia-Peña and R. P. Guillerman (eds.), Pediatric Chest Imaging, Medical Radiology. Diagnostic Imaging,DOI: 10.1007/174_2013_944, � Springer-Verlag Berlin Heidelberg 2013Published Online: 15 December 2013

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judicious ordering of imaging is the best method to decreaseexposure to ionizing radiation. When a chest radiograph isobtained, proper technique is important. Images are obtainedanteroposterior (AP) with the patient in the supine position.Care should be taken to avoid rotation. Imaging is centered atthe nipple line and should extend from the lung apicessuperiorly to L1/L2 level inferiorly. An AP view usuallysuffices for evaluation of the chest. Occasionally a cross-tablelateral view or a lateral decubitus view can be helpful, mostoften in the evaluation for an anterior pneumothorax.

3 Systematic Approach

A systematic method of evaluating radiographs is recom-mended. The lungs should demonstrate symmetrical aera-tion and radiolucency. Patient rotation will lead toasymmetrically increased or decreased density and a uni-lateral hyperlucent lung can mimic a pneumothorax or acongenital overinflation lesion. Pulmonary vasculatureshould be inconspicuous in the periphery of the lungs butshould be visible in the central two-thirds. The hemidia-phragms should be dome-shaped and the costophrenicangles should be sharp. The transverse cardiothoracic ratiocan be up to 60 % in neonates (Fig. 1). The normal thymuscan have a varied appearance and can mimic a mass orconsolidation. Various signs can be used to identify a nor-mal thymus. These include a wavy lateral border due to

impression by the anterior ribs, a notch between the thymusand the heart, and a sail-like appearance of the thymusprojecting off the mediastinum (Fig. 2). The thymus shouldbe visible in a normal neonate. However, stress and illnesscan lead to rapid involution of the thymus. Confirmation ofthe presence of a thymus and differentiation of a thymusfrom a mass can usually be made by ultrasound, as a normalthymus has a typical sonographic appearance (Fig. 3) (Hanet al. 2001).

Patients in the neonatal intensive care unit often havecatheters and tubes and evaluation of this support apparatus isan important part of reviewing chest radiographs in theseinfants. Review should include not only the chest cavity, butalso the osseous structures and the soft tissues of the chestwall. The upper abdomen should also be reviewed forcomorbid conditions such as necrotizing enterocolitis, acommon disease in patients with respiratory distress syn-drome (RDS) . The signs of this condition include pneuma-tosis intestinalis, portal venous gas, and free intraperitonealair, all of which may be identified on a chest radiograph(Fig. 4). Abdominal heterotaxy with malposition of thestomach and liver can be accompanied by asplenia or poly-splenia and is strongly associated with congenital heartdisease. The osseous structures need to be evaluated forvertebral and rib abnormalities. The Vertebral anomalies,Anal atresia, Cardiac anomalies, Tracheoesophageal abnor-malities, Renal anomalies, and Limb anomalies (VACTERL)

Fig. 1 Normal anteroposterior (AP) chest radiograph in a neonate.Symmetrically inflated lungs are seen with sharp costophrenic angles.The configuration of the cardiothymic silhouette is normal

Fig. 2 Thymic wave sign. Undulating lateral border of the softthymus from deformation by the overlying ribs. The thymus alsoprojects like a sail away from the other mediastinal structures

174 E. J. Crotty

association may be suggested by a dilated esophagus, absentbowel gas, and vertebral anomalies (Fig. 5). Rib anomaliescan be associated with conditions with restrictive physiologysuch as asphyxiating thoracic dystrophy and thanatophoric

dwarfism. In cases where the gestational age is unknown orwhere the provided history is limited, examination of thehumeri may help, as the proximal humeral epiphysis isossified in 80 % of term infants.

Fig. 3 Prominent thymus confirmed with ultrasound. a Neonate with a prominent lobulated mediastinal contour on a chest radiograph.b Ultrasound demonstrates a normal thymus with the typical appearance of echogenic lines and punctate foci on a hypoechoic stroma

Fig. 4 Abdominal pathology on a chest radiograph. Chest radiographin a 3 week old former 27 week gestation premature infant withnecrotizing enterocolitis demonstrating branching lucent structures inthe liver (arrowhead) consistent with portal venous gas

Fig. 5 VACTERL association. Notice the vertebral segmentationanomaly (white arrowhead). An enteric tube is coiled in the atreticproximal esophagus (black arrowhead) and there is gas in the bowelconsistent with esophageal atresia with a tracheoesophageal fistula.The patient also has a deformity of the left upper extremity

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4 Medical Disease

4.1 Transient Tachypnea of the Newborn

Transient tachypnea of the newborn (TTN), also known as‘‘wet lung,’’ is a common cause of respiratory distress ininfants who are either near-term, term, or postterm. It issecondary to retention of fetal fluid in the newborn’s lungand occurs with an incidence of 5.9 % (Tutdibi et al. 2010).

The production of fetal lung fluid decreases as gestationapproaches full term. The remaining fluid is cleared fromthe lungs during labor by active resorption of fluid from theair spaces through epithelial sodium channels. Hormones,including epinephrine, glucocorticoids, and thyroid hor-mones released during the stress of labor, as well as inhaledoxygen in the postnatal period trigger this resorptive pro-cess (Barker and Olver 2002). The removal of lung fluid ispractically completed by 2 h of life (Aherne and Dawkins1964). If the epithelial sodium transport mechanism isimmature or the lungs are not exposed to the stress of labor,fluid resorption may be inadequate. The retained fluid in theinterstitium leads to decreased compliance of the lungs. Themajority of this fluid is removed from the interstitium viathe pulmonary veins and lymphatics (Humphreys et al.1967; Bland et al. 1982). Epinephrine has also beendemonstrated to cause the release of surfactant (Lawsonet al. 1978), which increases pulmonary compliance anddecreases the effect of any retained fluid. Pressure trans-mitted to the lungs by compression of the chest wall duringdelivery with resultant clearance of fetal lung fluid via thetracheobronchial tree, the so-called ‘‘vaginal squeeze’’contributes minimally to removal of this fluid.

Transient tachypnea of the newborn is seen more often inpatients that are born by cesarean section, especially elec-tive cesarean section without preceding labor. It is also seenmore commonly in infants of mothers who have beensedated, in infants of diabetic mothers with poor glucosecontrol and in infants of mothers with asthma, in large orsmall for gestational age infants, and in male infants (Schatzet al. 1991; Persson and Hanson 1998; Tutdibi et al. 2010).The severity of TTN also correlates with elective cesareansection and shorter duration of labor as well as lower ges-tational age (Tutdibi et al. 2010).

Infants with TTN present with signs of respiratory distressand they may require supplemental oxygen. More severecomplications including pneumothorax, the need for positivepressure ventilation or extracorporeal membrane oxygena-tion, and death have been recorded (Ramachandrappa andJain 2008). The condition is usually self-limiting, mostpatients recovering in 24–72 h, but occasionally patientsneed longer to become asymptomatic. The majority ofpatients with TTN recover fully without long-term morbidity,

although some studies have shown an increased incidence ofchildhood asthma in these patients (Birnkrant et al. 2006).

Transient tachypnea of the newborn is a clinical diag-nosis and radiographs of the chest are primarily performedin these infants to exclude other causes of respiratory dis-tress. On imaging, the lungs are well inflated. Symmetri-cally prominent interstitial opacities radiating from the hilaare most commonly seen (Fig. 6). Diffuse fine granularopacities may be present bilaterally and can be confusedwith RDS if attention is not paid to the patient’s gestationalage and the degree of inflation. Small pleural effusions maybe evident, another finding not seen in RDS (Fig. 7). Afollow up radiograph is usually not indicated as the patientsclinically improve, but if performed it demonstrates rapidclearance of the radiographic abnormalities (Swischuk1970; Wesenberg et al. 1971).

4.2 Respiratory Distress Syndrome

Respiratory Distress Syndrome (RDS) is a disease of neo-nates resulting from surfactant deficiency. RDS is primarilya disease of premature infants born at less than 36 weeks ofgestation, although it can rarely be seen in term infants andalso in infants of diabetic mothers with poor glucose con-trol. Other factors that increase the risk of developing RDSinclude intrapartum asphyxiation, multiple gestation births,

Fig. 6 Term infant with transient tachypnea of the newborn. Thelungs are well inflated with prominent interstitial opacities radiatingfrom the hila. There is a small right pleural effusion (arrowheads)

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sepsis, and maternal and fetal hemorrhage. Male andCaucasian infants have an increased incidence of RDS(Anadkat et al. 2012). The lower the gestational age, thegreater the incidence of RDS; it occurs with an incidence of93 % in infants less than 28 weeks gestation (Stoll et al.2010), 10 % at 34 weeks, and 0.3 % at greater than38 weeks gestation (Hibbard et al. 2010).

Alveoli begin to form during the later part of the cana-licular stage of lung development, at about 24–28 weeksgestation (Agrons et al. 2005) and are lined by Type IIpneumocytes which express surfactant, a complex lipopro-tein, into the alveoli. Surfactant becomes activated when itcombines with surface surfactant proteins which are alsoproduced by Type II pneumocytes. This activated surfactantreduces surface tension within the alveoli, not only pre-venting them from collapsing but also allowing collapsedalveoli to expand with less applied force. In preterm infants,an insufficient amount of surfactant results in collapse of thealveoli and atelectasis with resultant development ofhypoxia and acidosis. An inflammatory reaction ensues,often exacerbated by oxygen therapy and barotrauma frompositive pressure ventilation. This inflammation results indamage to both the respiratory epithelium and capillaryendothelium with loss of integrity of these structures.Interstitial edema ensues along with formation of a mem-brane along the terminal bronchioles and alveolar ducts

(Stocker 1992). These hyaline membranes prevent gasexchange and result in ventilation–perfusion mismatching,leading to hypoxia and acidemia. Over time this can lead toarteriolar vasoconstriction and pulmonary hypertension.

Clinically, infants become symptomatic soon after birthand develop progressive worsening of symptoms over thefirst 48 h of life with signs of respiratory distress. Theincreased effort required for breathing leads to fatigue oftennecessitating support with positive pressure ventilation. Thenatural history for the majority of infants with uncompli-cated RDS is gradual improvement as endogenous surfac-tant production is induced. Superimposed neonatalpneumonia, a patent ductus arteriosus, persistent pulmonaryhypertension, and sepsis can all lead to prolongation ofsymptoms and a more complicated clinical course, includ-ing the development of an air leak. Long term, the infantsare at risk of developing bronchopulmonary dysplasia.

The administration of steroids to the expectant motherfor 12–36 h while in preterm labor has been shown toaccelerate lung maturation in fetuses over 28 weeks gesta-tion with decreased severity of RDS (Liggins and Howie1972). A similar decrease in the severity of RDS has notbeen shown to occur in infants born between 24 and28 weeks gestation following prenatal steroid administra-tion to the mother (Garite et al. 1992). However, infantsborn at this gestation have been shown to have a reducedincidence of other diseases of prematurity following steroidadministration, such as necrotizing enterocolitis, high-gradeintracranial hemorrhage, and also decreased mortality(Crowley et al. 1990). A further reduction in the severity ofRDS can be achieved by the administration of exogenoussurfactant to the neonate via an endotracheal tube (Sureshand Soll 2005). Exogenous surfactant therapy results indecreased surface tension in the alveoli and subsequentlessening of respiratory symptoms as the work of breathinglessens. In addition, the infant does not require as highconcentrations of therapeutic oxygen or as high positiveairway pressures if they are being mechanically ventilated.

The classic description of RDS on radiographs is diffusefine granularity bilaterally (Fig. 8), effacement of normalpulmonary vascularity, and central air bronchograms.Untreated lungs are low in volume due to the diffuse acinarcollapse (Fig. 9), although this is less commonly seen nowas patients are usually intubated, receive positive pressureventilation and are administered surfactant prior to an initialradiograph. Occasionally this may be more severe with nearcomplete whiteout of the lungs (Fig. 10). Followingadministration of surfactant and application of positive air-way pressure, these appearances may change, with improvedlung volumes and clearance of the diffuse granularity(Fig. 11). This improvement can be rapid and can result incomplete clearance, partial and symmetric clearance, orpatchy and asymmetric clearance (Dinger et al. 1997;

Fig. 7 Term infant with transient tachypnea of the newborn. Theappearance could be confused with respiratory distress syndrome asthere are fine granular opacities. However, the lungs are well inflatedand there is a small amount of pleural fluid along the minor pulmonaryfissure

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Fig. 8 Newborn with respiratory distress syndrome. a There are hazy opacities diffusely distributed bilaterally. b The granular nature of theseopacities is well seen on the magnified image

Fig. 9 Newborn with untreated respiratory distress syndrome. Thelungs are low in volume with increased density bilaterally and subtlecentral air bronchograms

Fig. 10 Newborn with a ‘‘whiteout’’ appearance from respiratorydistress syndrome. The lungs are densely opacified, obscuring thecardiac and diaphragmatic contours, and there are prominent airbronchograms bilaterally

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Slama et al. 1999), which may reflect uneven distribution ofthe administered surfactant, insufficient surfactant adminis-tration, and regional differences in aeration (Slama et al.1999) (Fig. 12). This uneven clearance can mimic otherentities such as neonatal pneumonia. Over time, the radio-graphic appearance may reflect complications of RDS andprematurity such as an air leak phenomenon, superimposedinfection, chronic lung disease related to the surfactantdeficiency, i.e., bronchopulmonary dysplasia, persistentpulmonary hypertension, and edema. This edema cansometimes be severe and hemorrhagic and is secondary to aleft-to-right shunt through a patent ductus arteriosus. Thiscan occur rapidly as pulmonary arterial blood pressuredecreases (van Houten et al. 1992). With treatment, local-ized hyperinflation can rapidly occur, mimicking air leaks(Cleveland 1995).

Very immature infants, less than 27 weeks gestation andweighing less than 1,000 g, may develop mild hazinessbilaterally which clears with surfactant therapy. Subse-quently, these infants may again develop mild diffuse haz-iness bilaterally, thought to reflect seepage of lung fluid intothe interstitium through damaged arteriolar basementmembranes, the so-called ‘‘leaky lung’’ (Swischuk et al.1996). Because these infants are extremely immature their

Fig. 11 Effect of surfactant administration. a Initial radiograph of anewborn with respiratory distress syndrome (RDS) taken followingintubation. Fine granular opacities are present bilaterally. b Radiograph

taken 12 h later demonstrates rapid clearing of these opacitiesfollowing the administration of surfactant

Fig. 12 Newborn premature infant with uneven aeration followingthe administration of surfactant. There is relative lucency in the rightupper lobe and relatively increased density in both lung bases

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lungs are hypoplastic with a deficient number of alveoli andas a result they often require prolonged positive pressureventilation and high oxygen concentrations. The resultantbarotrauma can lead to the early development of coarseirregular reticular opacities bilaterally consistent withchronic lung disease (Cleveland 1995) (Fig. 13).

Respiratory Distress Syndrome was formerly known asHyaline Membrane Disease, a term that is no longer favoredas hyaline membranes are seen in other neonatal lung dis-eases and are not specific to RDS. It has been suggested thatRDS is also a nonspecific descriptive term that coulddescribe the clinical appearance of a number of respiratoryillnesses and it has been proposed that the term SurfactantDeficiency Disease be used as this would more accuratelyreflect the underlying etiology (Swischuk and John 1996).

4.3 Bronchopulmonary Dysplasia

Bronchopulmonary dysplasia (BPD) is a chronic disorder ofthe lungs most commonly seen in low birth weight infantswho were born prematurely. The pathogenesis of BPD isnot completely understood but is complex and multifacto-rial in origin. Aside from prematurity, mechanical ventila-tion, and oxygen therapy, a number of other factors areknown to contribute to the development of BPD including apatent ductus arteriosus or fluid overload, inflammation

(alone or associated with infection), poor nutrition, andgenetics (Bancalari et al. 2003). Infection may result fromchorioamnionitis, may be acquired during delivery, or maybe nosocomial.

Bronchopulmonary dysplasia was originally described asa disease of premature infants who were treated with oxygenand mechanical ventilation (Northway et al. 1967). Theeffects from the surfactant deficiency coupled with the ven-tilator-induced lung injury and the further damage fromoxygen toxicity resulted in changes of alveolar septal fibrosis,alveolar cell hyperplasia, bronchiolar squamous metaplasia,and necrotizing bronchiolitis (Stocker 1986; Husain et al.1998). This resulted in heterogeneous airway and parenchy-mal disease with hyperinflated but otherwise normal alveolialternating with alveoli that are scarred to varying degreesalong with smooth muscle hypertrophy and airway damage.

The patient population in this original description of BPDpresented with severe RDS, had an average weight of 1,894 gand a gestational age of 33 weeks (Northway et al. 1967).Radiographically, this ‘‘old’’ BPD has four stages of devel-opment. Stage I (at 2–3 days) has changes of RDS with adiffuse granular pattern and central air bronchograms. StageII (at 4–10 days) demonstrates almost complete opacificationbilaterally. Stage III (10–20 days) shows small roundedlucencies with intervening areas of irregular opacification,while Stage IV ([1 month) has further enlargement of thelucent areas and thinning of the intervening linear opacitieswith hyperinflation of the lungs (Northway and Rosan 1968).These stages are less commonly seen today.

With modern therapy, a similar group of patients to thatdescribed in the initial description of BPD would have anexcellent prognosis and would be unlikely to develop BPD.However, the incidence of BPD is not decreasing. Thisreflects significantly increased survival rates of neonates ofless than 28 weeks gestation. Now the population that mostcommonly develops BPD has a gestational age of 22 to28 weeks and weighs as little as 500 g. The lungs of apatient with this ‘‘new’’ BPD are at a more immature andsimplified stage of development with fewer alveoli. Expo-sure to the extrauterine environment leads to a complete orpartial arrest in acinar development (Husain et al. 1998).This extreme immaturity coupled with the frequentadministration of prenatal maternal glucocorticoid therapyand postnatal extrinsic surfactant to the infant as well as lessaggressive positive pressure ventilation and oxygen therapy,has resulted in a different histological and radiographicappearance and has also resulted in changing definitions ofBPD. Currently the most widely accepted definition of BPDwas issued in 2001 following a workshop held by theNational Institute of Child Health and Human Develop-ment, the National Heart, Lung and Blood Institute, and theOffice of Rare Diseases (Jobe and Bancalari 2001). Thisdefines BPD as the need for supplemental oxygen for at

Fig. 13 Early development of chronic lung disease in a prematureinfant who is now 10 days of age. The lungs are hyperinflated andthere are coarse reticular opacities bilaterally with interveninglucencies. These findings are typical of chronic lung disease

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least 28 days following birth and its severity is gradedaccording to the extent of oxygen therapy and other respi-ratory support at 36 weeks postmenstrual age (gestationalage at birth plus chronologic age) or at discharge, whichevercomes first, if born at \32 weeks gestational age, or at56 days postnatal age or at discharge, whichever comesfirst, if born at 32 or [weeks gestational age.

The histology of this ‘‘new’’ BPD in these extremelypremature neonates demonstrates fewer but larger alveoliwhich have a more uniform caliber, with less interstitialinflammation and fibrosis. In these very immature neonates,chest radiographs initially may be clear or may demonstratesubtle diffuse hazy opacities bilaterally (Fig. 14). Overtime, because they have fewer alveoli than normal, theseneonates often require prolonged ventilator support andoxygen therapy. Although minimized, this support leads tochronic lung changes on chest radiographs. Most commonlythis is a diffuse haziness bilaterally (Fig. 15). Less com-monly they progress from this diffuse haziness to a moreheterogeneous appearance with diffuse cystic lucencies andcoarse reticular opacities bilaterally giving a ‘‘bubbly’’appearance to the lungs similar in appearance to stages IIIand IV of the original radiographic description of BPD. Thishas been described as developing within a week of birth(Swischuk et al. 1996) but may also occur later as describedin ‘‘old’’ BPD (Fig. 16) This appearance is seen wheninfants have a difficult post natal course that requires

Fig. 14 Newborn 24 week gestation premature infant, first day oflife. Mild hazy opacities are seen diffusely throughout both lungs

Fig. 15 Former 25 week gestation premature infant who is now70 days old. Note the diffuse hazy opacification throughout both lungs.This is consistent with ‘‘new’’ bronchopulmonary dysplasia

Fig. 16 Bronchopulmonary dysplasia in a 3-month-old former24 week gestation infant. The lungs are hyperinflated. Coarse reticularopacities are present bilaterally with intervening small roundedlucencies giving a somewhat ‘‘bubbly’’ appearance to the lungs

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intubation and high pressure ventilation and high concen-trations of supplemental oxygen.

CT is occasionally performed after the neonatal period inpatients with BPD. These studies are sometimes requestedin patients with ongoing respiratory difficulty in whom thereis concern for a comorbid condition such as aspiration. Ifperformed in infancy or early childhood, BPD will appearas hyperinflated lungs with distended secondary pulmonarylobules that are bounded by thickened interlobular septa(Fig. 17). Small subpleural cysts are frequently present. Thedistended secondary pulmonary lobules demonstrate airtrapping on expiratory images. If imaged later in childhood,patients with longstanding BPD demonstrate overallincreased lung volumes with mosaic attenuation and airtrapping. There are linear and band-like opacities thatrepresent areas of atelectasis and scarring. Subpleural tri-angular opacities that sometimes are associated with thelinear opacities are thought to represent pseudo-fissuring(Oppenheim et al. 1994) (Fig. 18).

4.4 Meconium Aspiration Syndrome

Meconium aspiration syndrome (MAS) is defined as respi-ratory distress in an infant born through meconium-stainedamniotic fluid with characteristic radiological changes and

Fig. 17 CT in a 4-month-old former 24 week gestation infant withBPD. a and b There are thickened interlobular septa (white arrow-head) surrounding distended secondary pulmonary lobules, some of

which are hyperlucent (arrow). Scattered subpleural cysts (blackarrowhead) are also present

Fig. 18 CT in a 5-year-old former 24 week gestation prematureinfant. Axial CT images demonstrates multiple linear bands (whitearrowheads), many extending to the pleural surface and manyassociated with triangular pleural-based opacities (black arrowheads).Subtle mosaic attenuation of the parenchyma is also present

182 E. J. Crotty

whose symptoms cannot be otherwise explained (Wiswellet al. 1990). MAS occurs when meconium is aspirated intothe lungs before or during labor and delivery. Staining ofamniotic fluid is seen in 8–20 % of births, with MASdeveloping in approximately 20 % of these cases (Ustaet al. 1995).

Meconium aspiration syndrome is a disease of term andespecially of postterm neonates and of small for gestationalage infants (Clausson et al. 1999). Passage of meconium inutero is rare before 37 weeks of gestation due to immaturityof the colon (Matthews and Warshaw 1979). Infants withMAS born after 40 weeks of gestation are more likely torequire intubation than those born earlier (Dargaville et al.2006). Factors predisposing to in utero passage of meconiuminclude advanced maternal age, placental insufficiency, fetaldistress, oligohydramnios, preeclampsia, and maternal druguse, particularly of cocaine (Swarnam et al. 2012).

Aspiration of meconium affects the lungs in a number ofways. If an airway is completely occluded, this can result inatelectasis. Partial occlusion of the airway may result in aball-valve phenomenon with hyperinflation of the portion ofthe lung that is distal to the meconium plug. This can resultin an air leak phenomenon if there is progressive overin-flation. Although the primary constituent of meconium iswater, it also contains many compounds such as pancreaticjuices, bile, and gastrointestinal secretions that irritate theairways and alveoli, resulting in a chemical pneumonitis.Although the aspiration may be focal, the influx ofinflammatory cells and chemical mediators in inflammationsuch as interleukins and tumor necrosis factors can induce amore widespread pneumonitis involving much of the lung(Cleary and Wiswell 1998). Surfactant lining the alveoli isdeactivated by meconium which also may decrease theamount of surfactant produced (Dargaville et al. 2001;Janssen et al. 2006). This combination results in surfactantdysfunction, further promoting atelectasis and diminishedaeration. The resultant hypoxia, hypercapnia, and respira-tory acidosis lead to pulmonary arterial vasoconstriction.This may be compounded by the effects of preexistingchronic intrauterine hypoxia leading to thickening of thearteriolar walls. The increased resistance in the pulmonaryvascular bed can result in persistent pulmonary hyperten-sion of the newborn (PPHN), further worsening the degreeof hypoxia and difficulty with ventilation.

Supplemental oxygen is the mainstay of therapy and maybe all that is required (Singh et al. 2009) but moreaggressive support is not unusual; intubation and mechan-ical ventilation is required in up to one-third of patients(Cleary and Wiswell 1998). In cases where adequate oxy-genation cannot be achieved with mechanical ventilation,extracorporeal membrane oxygenation may be needed.Surfactant therapy, corticosteroids, and nitric oxide havebeen used as adjuvant therapies (Dargaville 2012).

Over the past decades, a reduction in the risk of MAS hasbeen attributed to better obstetric practices, in particular, toavoidance of postmaturity and to expeditious delivery whenfetal distress has been noted (Yoder et al. 2002). However,the mortality in patients with MAS remains considerable at7 % (Dargaville et al. 2006), usually related to pulmonaryhypertension and cerebral hypoxic ischemic injury.Approximately 10 % of patients intubated for MAS willdevelop a pneumothorax. This is an indicator of diseaseseverity with a mortality rate of 42 % (Dargaville et al.2006).

The most significant long-term morbidity in MAS isneurological injury. A diagnosis of MAS in the neonatalperiod confers a considerable risk of cerebral palsy(5–10 %) and global developmental delay (15 %) (Beligereand Rao 2008). Pulmonary sequelae are also seen. In thefirst year of life, up to half of infants will demonstraterespiratory symptoms with wheezing and coughing (Yukselet al. 1993). Older children may exhibit evidence of airwayobstruction, hyperinflation, and airway hyperreactivity, butappear to have normal aerobic capacity (Swaminathan et al.1989).

On imaging a variety of appearances may be seen. Thelungs are usually well inflated. Some cases may demon-strate symmetric fine reticular opacities bilaterally or mayhave more streaky opacities in the perihilar regions bilat-erally, a radiographic appearance that can be difficult todifferentiate from TTN (Fig. 19). In more severe cases, thelungs are hyperinflated with coarser linear and band-likeopacities bilaterally reflecting atelectasis alternating withlucent areas corresponding to air trapping (Fig. 20). Moreill-defined confluent opacities can be seen and relate topneumonitis (Fig. 21). Findings may be symmetric but canbe quite asymmetric. Small pleural effusions may be present(Gooding and Gregory 1971) (Fig. 22). Because of diffi-culty with ventilation and adequate oxygenation, air leaksare not uncommon and result in pneumothorax and/orpneumomediastinum in approximately 10 % of patients(Wiswell et al. 1990). Depending on the severity of theaspiration, the findings may resolve within 48 h or they maypersist with more gradual improvement. However, theseverity of the appearances on imaging does not alwayscorrelate with the clinical findings.

4.5 Neonatal Pneumonia

Neonatal pneumonia results from infection that can arise bya number of routes. Infection can be acquired in utero eithertransplacentally or via an ascending infection of amnioticfluid, in the perinatal period by inhalation of infectedmaterial during or immediately following birth, or in theneonatal period. Predisposing factors to neonatal pneumonia

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Fig. 19 Mild changes of meconium aspiration. a and b Mildlycoarsened reticulonodular opacities are present bilaterally, mostprominent in the right perihilar region. Without the history of

meconium aspiration the appearance could be mistaken for transienttachypnea of the newborn or neonatal pneumonia

Fig. 20 Newborn term infant with meconium aspiration. The lungsare hyperinflated. Coarse reticulonodular opacities are presentthroughout both lungs with more confluent opacification in the rightupper lobe

Fig. 21 Meconium aspiration with pneumonitis. The lungs arediffusely abnormal bilaterally with confluent opacities in the rightmid lung and the left lower lobe. These confluent opacities areconsistent with areas of pneumonitis and atelectasis

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include prolonged rupture of membranes, chorioamnionitis,maternal vaginal colonization, prematurity, and prolongedhospitalization.

In the developing world, neonatal infection accounts forsignificant morbidity and mortality. WHO figures estimates800,000 neonatal deaths per year from respiratory infectionin developing nations (Garenne et al. 1992). The estimatedincidence in developed countries is less than 1 % in terminfants and closer to 10 % in preterm and low birth weightinfants (Dennehy 1987).

Neonatal pneumonia is termed as early onset if it man-ifests within the first 7 days of life, and the majority presentwithin 48–72 h. Early onset pneumonia, especially whenpresenting in the immediate postnatal period, is oftenassociated with generalized sepsis and a poorer prognosis.Pneumonia occurring beyond 7 days is considered late-onset, is usually not associated with sepsis, and generallyhas a better prognosis. Bacteria are the cause of most earlyand late-onset pneumonias.

The majority of early onset pneumonias in term andnear-term neonates are caused by group B beta hemolyticstreptococcus (GBS) , a common colonizer of the femalegenitourinary tract. The incidence of GBS pneumonia hasdecreased due to increased testing for GBS colonization ofthe mother’s genitourinary tract and increased use ofintrapartum antibiotics (Jeffery and Moses Lahra 1998).

Escherichia coli is now the most common cause of pneu-monia in very low birth weight infants (\1500 g) (Stollet al. 2005). Numerous other bacteria can cause ascendinginfection and include Hemophilus influenza, other gram-negative bacilli, Listeria monocytogenes, Enterococcus, andStaphylococcus. In very low birth weight infants, Urea-plasma urealyticum is frequently recovered from endotra-cheal aspirates shortly after birth. It has been associatedwith the development of early onset of chronic lung diseaseand a poor prognosis (Kotecha et al. 2004).Viral and fungalorganisms are rare causes of neonatal pneumonia. The mostcommon viral pathogens include herpes simplex virus,respiratory syncytial virus, and adenovirus.

Most late-onset pneumonias are also caused by bacteria.These infections are usually nosocomial, especially in pre-term infants, but can also be community-acquired followingdischarge. Organisms involved include Pseudomonasaeruginosa, E. coli, Streptococcus pyogenes, Staphylococ-cus aureus, and Streptococcus pneumoniae. Chlamydiatrachomatis, an obligate intracellular parasite, causes a late-onset pneumonia that can manifest between 4 and 12 weeksof age (Hammerschlag 1994).

Early onset neonatal pneumonia can present with non-specific signs of infection, including temperature instability,apnea or tachypnea, tachycardia or bradycardia, hypogly-cemia, abdominal distension, and listlessness. More specificsigns of respiratory infection including grunting, retractions,and nasal flaring are variably present. Infected neonatesmay be gravely ill as septicemia is common in early onsetpneumonia. In utero infection can result in the infant beingstill-born.

Chest radiographs in neonatal pneumonia are often non-specific as the appearance can overlap with other neonatalillnesses such as RDS, TTN, and meconium aspiration. Theradiographic appearance can also vary depending on theresponsible organism. As a consequence, the findings ofneonatal pneumonia on imaging can be quite varied andradiographic diagnosis is difficult especially if not correlatedwith the clinical setting. Unlike pneumonia in older children,an isolated focal consolidation is rare in neonatal pneumonia(Haney et al. 1984). Most commonly, radiographs demon-strate bilateral ill-defined air-space opacities (Fig. 23) butthese opacities can be diffuse and homogeneous (Haney et al.1984). Multifocal coarse opacities may also be seen, similarto meconium aspiration (Fig. 24). A pattern very similar toRDS with diffuse granular opacities with central air bron-chograms can be seen, usually with GBS infection (Ablowet al. 1976) (Fig. 25). However, small pleural effusions maybe present which suggest infection rather than surfactantdeficiency (Leonidas et al. 1977) (Fig. 26). In addition, thelungs are usually well inflated, rather than the low lungvolumes seen in RDS (Ablow et al. 1976). Chlamydia tra-chomatis pneumonia may be preceded by conjunctivitis.

Fig. 22 Meconium aspiration with an effusion. Coarse reticularopacities are present bilaterally. More focal opacities are present inthe peripheral left mid lung and in the left lower lobe with relativelucency at the right lung base suggesting air trapping. In addition, thereis a small right pleural effusion (arrowhead)

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Fig. 24 Neonatal pneumonia appearing like meconium aspiration.Bilateral coarse reticular and nodular opacities are present diffusely,most confluent in the left upper lobe. Washings from a bronchoalve-olar lavage isolated herpes simplex virus

Fig. 23 Neonatal pneumonia. The patient was born at 39 weeksgestation. The lungs are well inflated and there are diffuse finereticulonodular opacities bilaterally. More confluent opacities are seenin the bilateral upper and right lower lobes. Blood cultures grew groupB streptococcus

Fig. 25 Neonatal pneumonia appearing like respiratory distresssyndrome. There are diffuse symmetrical fine reticular and granularopacities bilaterally, findings that can be seen with respiratory distresssyndrome. However, the patient was a term infant and grew group Bstreptococcus from blood cultures

Fig. 26 Neonatal pneumonia and effusions. Fine reticular andgranular opacities are present bilaterally which suggest respiratorydistress syndrome. However, there are bilateral pleural effusions whichmake neonatal pneumonia more likely. Cerebrospinal fluid culturesgrew group B streptococcus

186 E. J. Crotty

Radiographs demonstrate hyperinflation with bilateralill-defined opacities, especially in the perihilar regions(Hammerschlag 1994) (Fig. 27).

5 Air Leak Phenomenon

Pulmonary air leaks occur when air escapes from the lunginto surrounding structures or compartments. Airwayoverdistension results in rupture of the alveoli and passageof air into the perivascular and peribronchial spaces,resulting in pulmonary interstitial emphysema (PIE) .Alternatively, it can track peripherally to the pleural surfaceand rupture into the pleural space to create a pneumothoraxor it can track centrally and enter the mediastinum to createa pneumomediastinum. Rarely, the air will track into thepericardial space to form a pneumopericardium, trackinferiorly into the abdomen to form a pneumoperitoneum,or enter one of the pulmonary veins and create an airembolus which can be rapidly fatal. An air leak most oftenoccurs as a result of intubation and mechanical ventilation.However, it can also occur in patients who only have hadcontinuous positive airway pressure (CPAP) applied(Fig. 28). Air leaks are most often associated with RDS,meconium aspiration syndrome, and conditions that causepulmonary hypoplasia.

5.1 Pulmonary Interstitial Emphysema

Pulmonary interstitial emphysema can compress the air-ways resulting in poorly compliant lungs that are difficult toventilate as they will not inflate and deflate with respiration.The increased pressure in the interstitium can also compresspulmonary veins resulting in impaired venous return anddiminished cardiac output (Plenat et al. 1978).

Radiographically, PIE is seen as tubular lucenciesextending towards the mediastinum and small cysticlucencies (Fig. 29). PIE can be unilateral or bilateral,focal or diffuse. Diffuse unilateral PIE can result inmediastinal shift into the collateral hemithorax. Occa-sionally the small cystic lucencies may coalesce into alarger focal intra-parenchymal lucency termed a pneuma-tocele (Fig. 30). Usually PIE resolves over time, but it canpersist and form a cystic mass that may result in masseffect and respiratory compromise and mimic a congenitalpulmonary airway malformation (Donnelly et al. 2003).Without clinical history and comparing to prior imaging,diffuse PIE may be difficult to differentiate from bron-chopulmonary dysplasia.

Fig. 27 Eight week old term female with chlamydia pneumonia. Thelungs are hyperinflated and there are coarse reticular opacitiesbilaterally with more focal opacities in the lingula

Fig. 28 Pulmonary interstitial emphysema in a patient on CPAP.Lucencies are seen throughout the left lung with intervening coarsereticular opacities. The patient was on continuous positive airwaypressure for respiratory distress syndrome and had never beenintubated

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5.2 Pneumothorax

When the air leak results in air entering the pleural space, apneumothorax is formed. The lung collapses toward thehilum and a sharp interface is seen between the collapsedlung and the air in the pleural space. If air enters the pleuralspace under positive pressure and cannot exit, a tensionpneumothorax may develop. This results in deviation of themediastinum to the contralateral side and flattening orinversion of the ipsilateral hemidiaphragm (Fig. 31). This isa potentially life threatening emergency as systemic venousreturn may be obstructed by the increased intrathoracicpressure. Obstruction to venous return may result in a nar-row appearance of the heart (Fig. 32). Fortunately, largetension pneumothoraces are easily identified. Less easilyappreciated are smaller pneumothoraces. This is especiallytrue in neonates in the intensive care setting as these imagesare obtained with the patient in the supine position. Thisresults in pleural air preferentially collecting anteriorly andmedially and an air-pleural interface may not be appreciableat the periphery of the lung (Moskowitz and Griscom 1976).On radiographs, a subtle lucency either focally or diffuselymay overlie the lung. Often this lucency is anteromediallypositioned and results in sharp margination of the heart,other mediastinal structures or the hemidiaphragm (Fig. 30).

Fig. 29 Diffuse bilateral pulmonary interstitial emphysema. a There are mixed lucencies and streaky opacities diffusely throughout both lungs.b On the magnified view, tubular lucencies are seen radiating from the hilum (arrows) as well as scattered cystic lucencies (arrowheads)

Fig. 30 Pulmonary interstitial emphysema and a pneumatocele.There is PIE and a rounded lucency in the right lung base consistentwith a pneumatocele (arrow). There is also a subtle left pneumothoraxindicated by overall mild decreased attenuation of the left hemithoraxas well as a lucency adjacent to the left heart border (arrowheads)

188 E. J. Crotty

Occasionally, the ipsilateral costophrenic angle may beasymmetrically prominent and well-defined, the ‘‘deep sul-cus sign’’ (Fig. 33). Confirmation of the presence or absenceof a pneumothorax may be obtained by performing a cross-table lateral or lateral decubitus view.

Occasionally skin folds can mimic the appearance of apneumothorax. On closer examination, they can usually becorrectly identified as the folds often extend beyond the edgeof the thoracic cavity and usually do not follow the expectedcontour of the lung edge (Fig. 34).

Spontaneous pneumothoraces that are not associatedwith pulmonary disease usually occur in the immediatepostnatal period. These are seen in 1 % of neonates withapproximately 10 % of these infants being symptomatic(Greenough et al. 1992).

5.3 Pneumomediastinum

If interstitial air tracks centrally, it can enter the mediastinumand form a pneumomediastinum. An isolated pneumomedi-astinum is usually not a clinical problem. Radiographsdemonstrate a lucent line sharply marginating the mediastinalstructures. In neonates the prominent thymus can be outlinedand occasionally elevated, giving a characteristic appearancethat has been termed the ‘‘angel wing’’ sign‘‘(Fig. 35). This isusually easily identified, but if the lobes of the thymus are

markedly displaced then they can simulate upper lobeopacification (Fig. 36). Another sign of a pneumomediasti-num is the ‘‘continuous diaphragm’’ signthat is seen when airis interposed between the diaphragm and the inferior surfaceof the heart. Mediastinal air, if extensive, can track superiorlyinto the neck or inferiorly into the peritoneal cavity (Fig. 37).

5.4 Pneumopericardium

Air tracking medially can enter the pericardial sac. A smallamount of air in the pericardial sac is very difficult todistinguish from pneumomediastinum. A large pneumo-pericardium is more easily differentiated from a pneumo-mediastinum as the air is confined to the pericardial sac,creating a focal lucency around the heart which does notextend beyond the confines of the pericardium (Fig. 38).The pericardium itself may be visualized as a thin stripeseparate from the surface of the heart. A large pneumo-pericardium can result in a pericardial tamponade anddecreased cardiac output. Very rarely, pulmonary interstitialair can enter the pulmonary veins and result in an airembolus that is often fatal.

6 Lines and Tubes

When evaluating a chest radiograph, it is important toclosely study the position of the support apparatus. Manypatients in neonatal care units have umbilical venous andarterial catheters (UVC and UAC, respectively), endotra-cheal tubes (ETT), and gastric tubes, and malpositioning ofthese devices can lead to complications with resultant pro-longed hospital stay, long-term morbidity, and even death.It can be easy to overlook the position of these devices,especially when they overlap or when there are confoundingdistractions like external wires and leads.

A correctly placed umbilical venous catheter follows thesingle anteriorly positioned umbilical vein that coursescephalad from the umbilicus into the liver along the freeedge of the falciform ligament, usually at or slightly to theright of midline. Within the liver, the umbilical vein inter-sects with the left branch of the portal vein before contin-uing cranially as the ductus venosus to the middle or lefthepatic vein, ultimately draining into the inferior vena cava(IVC) and right atrium. Optimal positioning of the tip of aUVC is below the right atrium within the suprahepatic IVC,between the T9 and T12 vertebral body levels (Fig. 39).A UVC can take an abnormal course prior to reaching itsoptimal position in the IVC or it can be advanced beyondthe IVC. Abnormal positions prior to reaching the IVCinclude within the right or left branches of the portal vein(Fig. 40), the main portal vein, the superior mesenteric vein

Fig. 31 Respiratory distress syndrome complicated by a tensionpneumothorax. The left hemidiaphragm is flattened (arrows) and themediastinal structures are displaced into the right hemithorax

Neonatal Chest Imaging 189

Fig. 32 Bilateral tension pneumothoraces with impaired venousreturn. Both hemidiaphragms are inverted and the heart has a narrowconfiguration (arrowheads) related to diminished central venous return

Fig. 33 Deep sulcus sign. Notice the asymmetric lucency of the righthemithorax, the lucent margination of the right side of the medias-tinum and right hemidiaphragm, and the deeper than usual appearanceof the right costophrenic sulcus (arrowhead)

Fig. 34 Skin folds mimicking a pneumothorax. Relative lucency isseen in the periphery of the right hemithorax, raising the concern for apneumothorax. However, the ‘‘edge’’ of the air-soft tissue interface canbe followed beyond the ribs and into the chest wall (arrowheads),consistent with a skin fold. On closer inspection, multiple skin foldsare visible along the right chest wall

Fig. 35 Pneumomediastinum and angel wing sign. There is a lucentband outlining the right side of the superior mediastinum andextending under the right lobe of the thymus, slightly elevating itfrom the heart (arrowheads). A slightly more exaggerated appearanceis seen on the left side. The elevated thymic lobes have theconfiguration of ‘‘angels’ wings’’

190 E. J. Crotty

Fig. 36 Lobes of thymus simulating upper lobe opacification. Thelobes of the thymus are lifted superiorly away from the heart and couldbe mistaken for upper lobe opacities. The apical position of the leftthymic lobe could also be mistaken for a loculated pleural effusion

Fig. 37 Newborn premature infant with pneumoperitoneum second-ary to a pneumomediastinum. Air has collected centrally in themediastinum (black arrowheads) and has extended inferiorly into theabdomen (black arrow) and into the neck (white arrowhead)

Fig. 38 Pneumopericardium. Interstitial air has tracked centrally andentered the pericardial sac, surrounding the heart. Note the airoutlining the left atrial appendage (arrowhead)

Fig. 39 Appropriate positioning of umbilical arterial and venouscatheters. The tip of the UAC (black arrowhead) is at the level of theT7 vertebral body and the tip of the UVC (white arrowhead) is atthe level of the suprahepatic IVC

Neonatal Chest Imaging 191

(Fig. 41), or the splenic vein. There is increased likelihoodof the UVC being abnormally positioned if it loops in theliver (Fig. 40). This looping often occurs in the umbilicalrecess , a dilated segment of the umbilical vein situatedimmediately prior to the junction with the left portal vein.Abnormal positioning of a UVC in a portal vein may causedamage to the liver from the infused fluids. The UVC canalso perforate the hepatic venous structures and terminate inthe liver parenchyma.

If the UVC is advanced too far then it may terminate inthe right atrium or, progress through the foramen ovale intothe left atrium and from there into the left upper pulmonaryvein (Fig. 42). Rarely, it may pass through the tricuspidvalve into the right ventricle (Fig. 43) and from there it mayenter the pulmonary arterial system. Alternatively, it maytraverse the right atrium and enter the central veins abovethe heart (Fig. 44).

A correctly placed UAC follows one of the pairedumbilical arteries which course caudad and posteriorly fromthe umbilicus to the internal iliac arteries. The UAC passesinto the internal iliac artery, then the common iliac arteryand aorta. Favored positioning of the tip of the UAC isbetween the T6 and T10 levels, proximal to the origin of theaortic branches that supply the abdominal organs (Fig. 39).

Fig. 40 Abnormal position of umbilical arterial and venous catheters.The UAC loops back on itself within the aorta (white arrowhead).Having looped in the umbilical recess, the UVC courses into the rightportal vein (black arrowhead)

Fig. 41 Abnormal position of an umbilical venous catheter. Thecatheter courses inferiorly along the main portal vein to terminate inthe superior mesenteric vein (arrowhead)

Fig. 42 Umbilical venous catheter in the left upper pulmonary vein.The UVC has crossed through a patent foramen ovale into the leftatrium and then into the left upper pulmonary vein (arrowhead)

192 E. J. Crotty

If this position cannot be obtained, then the catheter tip maybe positioned below the origin of these branches betweenthe L3 and L5 vertebral body levels. The high position ispreferred because it is associated with a lower incidence ofcomplications, such as thrombosis (Mokrohisky et al.1978). Abnormal positioning of the UAC includes loopingin the aorta (Fig. 40) or positioning in the ipsilateral orcontralateral common iliac, external iliac, or femoral artery,or within a branch of the abdominal aorta.

Endotracheal tubes should be positioned in the intra-thoracic trachea above the carina. Positioning too high inthe trachea increases the risk of accidental extubation. Alow position of the ETT may cause collapse of the contra-lateral lung (Kuhns and Poznanski 1971) (Fig. 45) oroverinflation of the ipsilateral lung with a resultantincreased risk of an air leak (Thibeault et al. 1973). Unin-tended intubation of the esophagus can be recognized bygaseous distension of the esophagus, stomach, and bowelwith volume loss of the lungs (Fig. 46).

Nasogastric and orogastric tubes should follow the courseof the esophagus and terminate in the stomach. Occasion-ally, they may terminate in the esophagus or be ectopicallypositioned in the tracheobronchial tree (Fig. 47). If thesetubes are used to administer nutrition, then positioning in the

Fig. 43 Umbilical venous catheter in the right ventricle. The UVChas looped in the right atrium and courses through the tricuspid valve,terminating in the right ventricle (arrowhead)

Fig. 44 Umbilical venous catheter above the heart. The catheter hasbeen advanced through the right atrium and terminates in the rightbrachiocephalic vein (arrowhead)

Fig. 45 Endotracheal tube in the right mainstem bronchus. Theendotracheal tube has been advanced beyond the carina into the rightmainstem bronchus, resulting in collapse of the left lung

Neonatal Chest Imaging 193

tracheobronchial tree or esophagus may lead to aspirationand chemical pneumonitis. Esophageal perforation canoccur, usually at the level of the piriform sinuses, especiallyin premature infants (Sapin et al. 2000).

7 Summary

Imaging of neonatal lung disease continues to play animportant role in the care of ill infants. Although theradiographic appearances of many of the conditions canoverlap, the clinical history including gestational age,maternal history, and birth history combined with theradiographic findings most often allow the radiologist tocorrectly diagnose the patient’s illness. Attention to thesupport apparatus as well as extra-pulmonary findings is animportant part of image interpretation.

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